Evidence map›Paper›PMID 27980230›Full record

ArticleOncotarget2017

A childhood acute lymphoblastic leukemia-specific lncRNA implicated in prednisolone resistance, cell proliferation, and migration.

Manon Ouimet, Simon Drouin, Mathieu Lajoie, Maxime Caron, Pascal St-Onge, Romain Gioia, Chantal Richer, Daniel Sinnett

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.0field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 44 citations in OpenAlex.

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  12. Non-Coding RNA Signatures of B-Cell Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2021
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  20. Long Non-Coding RNA and Acute Leukemia.International journal of molecular sciences · 2019
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Manon OuimetDivision of Hematology-Oncology, Research Center, Sainte-Justine University Health Center, Montreal, QC, Canada.
Simon DrouinDivision of Hematology-Oncology, Research Center, Sainte-Justine University Health Center, Montreal, QC, Canada.
Mathieu LajoieDivision of Hematology-Oncology, Research Center, Sainte-Justine University Health Center, Montreal, QC, Canada.
Maxime CaronDivision of Hematology-Oncology, Research Center, Sainte-Justine University Health Center, Montreal, QC, Canada.
Pascal St-OngeDivision of Hematology-Oncology, Research Center, Sainte-Justine University Health Center, Montreal, QC, Canada.
Romain GioiaDivision of Hematology-Oncology, Research Center, Sainte-Justine University Health Center, Montreal, QC, Canada.
Chantal RicherDivision of Hematology-Oncology, Research Center, Sainte-Justine University Health Center, Montreal, QC, Canada.
Daniel SinnettDivision of Hematology-Oncology, Research Center, Sainte-Justine University Health Center, Montreal, QC, Canada.
Centre Hospitalier Universitaire Sainte-Justine · CAUniversité de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Childhood acute lymphoblastic leukemia (cALL) is the most common pediatric cancer and, despite an 85% cure rate, still represents a major cause of disease-related death in children. Recent studies have implicated long non-coding RNAs (lncRNAs) in cALL etiology, progression, and treatment response. However, barring some exceptions little is known about the functional impact of lncRNAs on cancer biology, which limits their potential as potential therapeutic targets. We wanted to investigate the functional role of lncRNAs identified as specifically overexpressed in pre-B cALL by whole-transcriptome sequencing. Here we report five lncRNAs specifically upregulated in pre-B cALL that had significant impacts on cancer hallmark traits such as cell proliferation, migration, apoptosis, and treatment response. In particular, silencing of the RP11-137H2.4 lncRNA effectively restored normal glucocorticoid (GC) response in a GC-resistant pre-B cALL cell line and specifically modulated expression of members of both the NRAS/BRAF/NF-κB MAPK cascade and cell cycle pathways. Since GC form the cornerstone of cALL chemotherapy and resistance in cALL confers a dismal prognosis, characterizing RP11-137H2.4'sexact role and function in this process will be critical to the development of new therapeutic approaches to overcome GC resistance in children treated for cALL.

Indexed as

Antineoplastic AgentsApoptosisCell CycleCell Cycle ProteinsCell Line, TumorCell MovementCell ProliferationChildChild, PreschoolDrug Resistance, NeoplasmFemaleGene Expression Regulation, LeukemicHumansMaleMAP Kinase Signaling SystemPrecursor B-Cell Lymphoblastic Leukemia-LymphomaAntineoplastic AgentsCell Cycle Proteinslong noncoding RNA RP11-137H2.4, humanPrednisoloneRNA, Long Noncodingacute lymphoblastic leukemiaglucocorticoidslong non-coding RNARNASeqtreatment resistance

Identifiers

PMID27980230
PMCPMC5352336
OpenAlexW2564570500

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.